Equine encephalitis has been around for a long time. Old-time horsemen simply referred to it as sleeping sickness. They knew that if a horse contracted it, the animal's prognosis was not great, and that if he did recover, his ability to perform might be compromised. While these horsemen were basically correct in their categorization, this is not a simple malady. For example, there are at least six different viruses that can cause equine encephalitis or neurologic disease. They are identified as Eastern equine encephalitis (EEE), Western equine encephalitis (WEE), Venezuelan equine encephalitis (VEE), West Nile virus (WNV), the neurologic form of equine herpes virus (EHV-1), and rabies. In this article, we will concentrate on the first four, because they all have one thing in common--for the most part they are transmitted by insects.

First, however, there's the matter of nomenclature. What is the difference between encephalitis and encephalomyelitis? Encephalitis, according to Dorland's Medical Dictionary, involves "inflammation of the brain," while encephalomyelitis is "inflammation involving both the brain and the spinal cord."

In this article we'll use the term encephalitis because in the diseases discussed, there is almost always inflammation of the brain, but in some there might not be inflammation of the spinal cord.

EEE, WEE, VEE, and WNV are transmitted via mosquitoes, which usually pick up the respective viruses from birds and can pass it on to horses, humans, and other vertebrate species. For some time, there was concern that the horse could be an amplifying host for these viruses. In other words, if a mosquito bit an infected horse, then bit a human, there was concern that the disease could be transmitted to humans in that manner.

Science has proven that to be mostly incorrect, says R.D. (Dean) Scoggins, DVM, former equine extension veterinarian at the University of Illinois College of Veterinary Medicine. (Scoggins has officially retired, but remains with the Illinois school on an emeritus basis.) The only exception is VEE, which can cause viremia (presence of virus in the bloodstream) high enough in a horse for the virus to be picked up by mosquitoes and passed to other species, including humans.

The type of birds that serve as reservoirs for the encephalitis viruses appear to vary by geographic location. In Illinois, says Scoggins, the pheasant is often a culprit for EEE virus. In New Jersey, according to Wayne J. Crans, PhD, research professor in entomology at Rutgers University, EEE virus infection occurs naturally in a wide variety of wild songbirds. Blood samples from New Jersey birds, he reports, indicate that blue jay, wood thrush, tufted titmouse, chickadee, catbird, and cardinal show the highest incidence of infection in the state. Not all of these species are necessarily reservoir hosts.

One of the problems in preventing or eliminating an encephalitis virus is that the virus can survive for a long period of time in a bird, even over winter when no mosquitoes are around to serve as vectors. Some of the bird species that can carry the virus are migratory and thus are capable of spreading the disease over diverse geographic areas.

"This is a disease of the summer and fall, primarily because it is related to the period of the year of maximal vector activity," Scoggins says.

Crans states that mosquitoes transmit the infection from bird to bird during the early summer months in New Jersey, and that infections usually peak some time in August. In some years, he says, the virus remains in local bird populations and does not pose a health threat to horses or humans. However, when mosquito populations are high, and there is virus build-up in those populations, then transfer from birds to horses and/or humans can occur.

The bad news is that little can be done once a horse contracts encephalitis. "Because it is a viral disease, we do not have any anti-viral drugs that are effective in treating it," says Scoggins. "Treatment is all symptomatic, making sure horses get the nutrition they need and using anti-inflammatory drugs to control fever and inflammatory changes in the central nervous system."

Another bit of bad news is horses which do recover often are never quite the same as they were before contracting the disease. In other words, they can be left with various neurologic deficits.

"Those horses which recover from encephalitis are often called dummy horses," Scoggins said. "Mares often will not be good mothers, and they are often not safe to ride or to compete if they have been through a severe bout of the disease, particularly the Eastern form. This is due to the permanent damage that has occurred to the brain."

It appears that the same can be true of horses which have suffered from West Nile virus. At the 2003 AAEP convention in New Orleans, La., Julia Wilson, DVM, of the University of Minnesota, presented a report that indicates many horses which have suffered from WNV do not completely recover. The Minnesota study was conducted, Wilson says, because little information was available regarding the quality of horses' recovery from the illness and return to full function.

She adds that an assessment of equine cases in Florida suggests that 15% of the survivors did not completely regain neurologic soundness. However, she reports, preliminary observations and follow-up of a number of confirmed WNV cases in Minnesota in 2002 (992 cases were reported in the state) suggest that an even greater percentage of horses suffered long-term effects from the illness.

During early 2003, Wilson says, questionnaires were mailed to owners of horses which had suffered from WNV. At the time of her report, some 200 questionnaires had been mailed out and 131 had been returned. Six of the returned questionnaires were not used in the study because the horse had either died or been euthanized during the acute illness.

Here is what Wilson says about the study, as published in the AAEP Proceedings:

"One hundred and two of the 125 horses (81.6%) were considered by the owner to be fully recovered, but only 13 had been re-evaluated by a veterinarian. Despite the owner's opinion that a horse had fully recovered, only 74 of these (59.2%) had no currently observable neurologic or behavioral abnormalities. Residual deficits that were described in horses which owners deemed to have fully recovered were predominately gait and behavioral abnormalities (28 horses)."

Sixteen (12.8%) of the horses, according to Wilson, were described as having a single abnormality. They were broken down like this--behavioral change, 8; loss of muscle mass, 2; more frequent stumbling, 2; diminished energy level, 2; weak hind limbs, 2.

Twenty-two of the 125 horses (17.6%) in the study were described by their owners as having incomplete recoveries, and one was undecided because the horse had not returned to work yet.

Gait abnormalities were described for 17 of the 22. Fifteen of the 22 also were reported to have behavioral changes. There appeared to be no distinct pattern to the behavioral changes. Wilson says, "The behavioral changes commonly described by the owners were predominantly of three types--change in demeanor, change in mental abilities, and abnormal behavior patterns. Five horses were described as becoming very quiet and calm. A similar number became more easily startled or spooked. Three horses became more irritable, and one previously calm horse became very agitated when asked to give even small children a short ride at a walk. Five horses developed what the owners perceived as loss of memory or vision. One horse had a single brief seizure after a trail ride, and two horses had episodes of sudden onset of sleepiness suggestive of narcolepsy.

"The results of this survey of horses recovering from infection with West Nile virus suggest that it will be difficult for veterinarians to give clients an unreserved, good prognosis for recovery from this disease. Forty percent of the horses in this dataset still experienced either behavioral changes or gait abnormalities--or both--at approximately six months post-diagnosis."

Vaccinations

The story is not one of all doom and gloom. There is a bright spot in the form of vaccines to prevent horses from contracting encephalitis when bitten by an infected mosquito. Vaccines against EEE, WEE, and VEE have been around for a long time and are proven to be effective. The WNV vaccines are relatively new because the disease did not surface in this country until 1999.

Some 14,717 horses from 40 states were afflicted with WNV in 2002, according to Maureen Long, DVM, PhD, Dipl. ACVIM, of the University of Florida. The general assumption among researchers is that the number would have been much greater without use of the then-available vaccine.

In addition, there has been anecdotal evidence that some vaccinated horses which contracted WNV had a milder form than horses not vaccinated.

"The problem," says Scoggins, "is that as horse owners we want the vaccine to be perfect, and there is very little of anything that is perfect."

Vaccines against WEE, EEE, and VEE, he believes, have stood the test of time, and that the same will ultimately be true of the WNV vaccine. Scoggins has this to say about the EEE, WEE, and VEE vaccines, which, he says, should be administered well in advance of the mosquito season so that proper levels of immunity are developed in time: "Horse owners need to be aware that the vaccines are highly effective. If there is a problem with the vaccines, it is that the immunity they provoke is not long-lasting. Horses that are vaccinated prior to May 1 in a summer with excessive numbers of mosquitoes need to think about re-vaccination in August or September. It is important to use at least a bivalent vaccine (one with protection against Western and Eastern forms). Horses traveling to places where Venezuelan encephalitis has occurred should use a trivalent vaccine (protection against all three diseases). The vaccines are safe to use in horses at all ages. Initial vaccination of foals in endemic areas should be at three to four months of age."

Veterinarians recommend that WNV vaccines be administered well in advance of the mosquito season at the intervals suggested in order to establish immunity. In areas like Florida, where mosquitoes are active for much of the year, additional booster shots during the season are recommended.

Following is a rundown of the four types of encephalitis that are generally caused by insect vectors--West Nile virus, Western equine encephalitis, Eastern equine encephalitis, and Venezuelan equine encephalitis.

West Nile Virus

Much of what follows is contained in an informational treatise on the disease released by Pennsylvania State University. It provides a brief review and a discussion about prevention.

West Nile virus first reared its head in Africa in 1937 when the first human case was reported. It has since been found in Asia, Europe, and the Middle East, as well as making its way to the United States.

The disease was detected for the first time in the United States in August of 1999. The first outbreak in this country occurred in the New York City metropolitan area, where 62 people were diagnosed initially with the disease in that year. Seven of them died. The infection also was diagnosed in several breeds of horses, a variety of zoo birds, and various native bird species, especially crows.

In October of that year, the United States Department of Agriculture and the Centers for Disease Control and Prevention confirmed that 25 horses had signs of WNV encephalitis (nine died). That was the beginning. The disease then began its spread across the United States and continues on a westward course today.

As mentioned earlier, mosquitoes become infected after taking a blood meal from an infected bird. They, in turn, infect horses after biting them. The incubation period--the time between exposure to the virus and appearance of the first signs of the disease--is between five and 15 days.

As is the case with WEE, EEE, and VEE, no curative treatment of infected horses exists because no specific antiviral agents have yet been identified that act upon WNV. The case-fatality rate is around 30% in horses.

Following are suggestions from Penn State on preventing transmission of WNV, in addition to vaccination. The suggestions also apply for the other three forms of mosquito-borne encephalitis.

Place incandescent bulbs about 50 yards from the stable to attract mosquitoes away from horses. Black lights are of little value as attractants for mosquitoes.

Prevent pigeons and other birds from roosting and living in or near the stables.

Periodically examine the property for dead birds, particularly crows, blue jays, and raptors (hawks and owls). Handle dead birds only if wearing protective gloves and place birds in plastic bags.

Carefully examine your property and eliminate locations that could serve as breeding grounds for mosquitoes. Shallow, stagnant, or standing water, used tires, and manure storage pits are ideal places for mosquitoes to breed.

Clean water troughs weekly and pay attention to puddles that form around and under the troughs. Consider using stone or landscaping to reduce or eliminate hoof prints where mosquitoes might breed.

Topical preparations containing mosquito repellents are available for horses. Read the label before using the product and follow all instructions.

Stable premises can be fogged in the evening to reduce the number of mosquitoes.

Eastern Equine Encephalitis

Much of the following is from information disseminated by Crans. As the name implies, EEE is found primarily in the Eastern part of the United States and rarely is found in the Midwest and West. Generally speaking, EEE is found along the Eastern seaboard from New England to Florida. It generally kills affected horses--the case-fatality rate ranges between 75-100%.

The disease can also affect humans, but, unlike WNV, this is rare. When humans do contract EEE, the probability of recovery is less than 50%.

The virus that causes EEE can't pass from horses to humans by contact, body fluids, or any other physical mechanism. While a sick horse does not pose a health threat to his human owners, he does serve as a wake-up call that the local bird population is circulating the virus and that local mosquitoes are contracting infection.

In a fact sheet he prepared, Crans says, "The virus that produces EEE is widespread in wild bird populations and preventive vaccination is the only method available to protect horses from the disease. Vaccinations should be administered by a licensed veterinarian to ensure that viable vaccine is utilized and that injections are properly administered. Mistakes in vaccination protocol by well-meaning horse owners can result in ineffective protection in an animal that was thought to be risk-free.

"All too frequently, owner-vaccinated horses develop overt disease, indicating that the animal was improperly vaccinated or was vaccinated with a vaccine that had lost its protective properties," Crans continues. "Properly administered vaccinations are effective for only one year, thus, booster shots are required on an annual basis. Newly vaccinated animals require a two-shot series administered two to four weeks apart before protection can be established. Foals should be re-vaccinated during summer to ensure protection during the first year of life. In the face of a fall epidemic, it is recommended that horses vaccinated in March should be boostered later in the season."

Clinical signs of EEE are essentially similar to those for the other forms of encephalitis. Clinical signs include depression, lack of muscular coordination, weakness, circling, head tilt, paralysis, muscle tremors, and convulsions. When such signs appear, the horse owner should immediately contact a veterinarian. Blood and tissue samples can be tested to confirm a diagnosis. Euthanasia might be necessary because the disease generally is fatal in unvaccinated horses.

Western Equine Encephalitis

As the name implies, this form of encephalitis is found in the Western part of the United States--normally west of the Mississippi river. It is, says Scoggins, the form of encephalitis that is least fatal in horses. Yet, statistics indicate that the case-fatality rate generally ranges between 20-50%. One particular species of mosquito--Culex tarsalis--is implicated as being the vector that is responsible most of the spread of WEE. C. tarsalis feeds primarily on house sparrows and house finches.

While many horses with WEE exhibit signs of "sleeping sickness," some become agitated and excitable. They may become frenzied after any type of stimulation.

In cases where death is the final outcome--and this would be true in WEE, EEE, and VEE--the horse might become recumbent and comatose for a day to a week. Animals which survive an attack generally show gradual improvement of function over weeks or even months.

Venezuelan Encephalitis

Scoggins describes VEE as the most lethal form of the equine encephalitides and currently exotic to the United States. The greatest risk, he says, is in the southern tier of states. The last time the disease occurred in this country was in 1971, when it spread into Brown County in southern Texas from Mexico. VEE was first diagnosed in Venezuela in 1936.

While it is much like EEE, WEE, and WNV as far as signs are concerned, there is an additional aspect to VEE. With VEE, horses are not dead-end hosts. Aside from the high viremias (levels of virus in the bloodstream) that it can cause, VEE virus can be present in saliva and nasal discharges and can be spread to other horses and possibly even to people by means other than mosquito bite.

Most horses which contract VEE end up dead.

Take-Home Message

As mentioned earlier, there is good news. Although encephalitis is a deadly affliction, steps can be taken to prevent it. Perhaps the most important step is immunization. Just what that immunization program should entail can vary geographically and is something that should be discussed with a veterinarian well in advance of mosquito season. Add proper facility and horse management to your vaccination program, and you likely can help your horses avoid these deadly maladies.

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